Lipid peroxidation product

Palozza, P. et al., Dual role of beta-carotene in combination with cigarette smoke aqueous extract on the formation of mutagenic lipid peroxidation products in lung membranes dependence on pOj, Carcinogenesis, 2006. 

Claxson, A.W.D., Hawkes, G.E., Richardson, D.P., Naughton, D.P., Haywood, RM., Chander, C.L., Atherton, M., Lynch, E.J. and Grootveld, M.C. (1994). Generation of lipid peroxidation products in culinary oils and frits during episodes of thermal stressing a high field H NMR study FEBS Lett. 355, 81-90. 

Esterbauer, LI. (1985). Lipid peroxidation products formation, chemical properties and biological activation. In Free Radicals in Liver Injury (eds. G. Poli, K. Cheeseman, M.U. Dianzani and T. Slater) pp. 29-47, IRL Press, Oxford. 

Although atherosclerosis and rheumatoid arthritis (RA) are distinct disease states, both disorders are chronic inflammatory conditions and may have common mechanisms of disease perpetuation. At sites of inflammation, such as the arterial intima undergoing atherogen-esis or the rheumatoid joint, oxygen radicals, in the presence of transition-metal ions, may initiate the peroxidation of low-density lipoprotein (LDL) to produce oxidatively modified LDL (ox-LDL). Ox-LDL has several pro-inflammatory properties and may contribute to the formation of arterial lesions (Steinberg et /., 1989). Increased levels of lipid peroxidation products have been detected in inflammatory synovial fluid (Rowley et /., 1984 Winyard et al., 1987a Merry et al., 1991 Selley et al., 1992 detailed below), but the potential pro-inflammatory role of ox-LDL in the rheumatoid joint has not been considered. We hypothesize that the oxidation of LDL within the inflamed rheumatoid joint plays a pro-inflammatory role just as ox-LDL has the identical capacity within the arterial intima in atherosclerosis. 

Evidence that oxidized lipids play a role in the pathogenesis of RA comes from studies demonstrating the presence of lipid products arising from radical attack in rheumatoid synovial fluid. This is consistent with oxidation reactions occurring locally in the joint. Lipid peroxidation products that react with thiobarbituric acid (TBARs) have been detected in rheumatoid knee-joint synovial fluid (Rowley et /., 1984). In addition, the... 

Babizhayev, M.A. (1989b). Accumulation of lipid peroxidation products in human cataracts. Acta Ophthalmol. 67, 281-287. 

Isolated hepatocytes incubated with ionic iron rapidly undergo lipid peroxidation. Some studies have not shown a consequent decrease in viability (as indicated by uptake of trypan blue or release of enzymes). This is probably a result of short incubation times, as changes in viability lag behind increases in lipid peroxidation, and may not occur for more than 2 h after lipid peroxidation begins (Bacon and Britton, 1990). Recent studies have shown strong correlations between increased lipid peroxidation [production of thiobarbituric acid (TBA) reactants] and loss of cell viability (trypan blue staining) (Bacon and Britton, 1989). The significance of the lag between lipid peroxidation and decreases in cell viability is as yet uncertain. 

Repeated periods of exercise reduce the likelihood of damage to skeletal muscle during subsequent bouts of the same form of exercise and this appears to be associated with an increase in the activity of muscle SOD (Higuchi et al. 1985), a reduced level of lipid peroxidation products during exercise in trained rats (Alessio and Goldfarb, 1988), and a modification of the concentration of antioxidants and activity of antioxidant enzymes in trained humans (Robertson etal., 1991). Packer and colleagues (Quintanilha etui., 1983 Packer, 1984) have also examined the exercise endurance of animals of modified antioxidant capacity and found that vitamin E-deficient rats have a reduced endurance capacity, while Amelink (1990) has reported that vitamin E-deficient rats have an increased amount of injury following treadmill exercise. 

Atheromatous plaques are loaded with lipid peroxide products... 

Antioxidants may intervene at any of the three major steps of the oxidative process initiation (oxygen consumption), propagation (conjugated dienes and peroxides formation), or termination (lipid peroxidation products). 

Oxidative damage to membrane polyunsaturated fatty acids leads to the formation of numerous lipid peroxidation products, some of which can be measured as index of oxidative stress, including hydrocarbons, aldehydes, alcohols, ketones, and short carboxylic acids. 

Hughes H, Smith CV, Tsokos-Kuhn JO and Mitchell JR. 1986. Quantitation of lipid peroxidation products by gas chromatography-mass spectrometry. Anal Biochem 152(1) 107—112. 

As mentioned earlier, MPO-hydrogen peroxide-chloride system of phagocytes induces the formation of lipid peroxidation products in LDL but their amount is small [167-169], It was proposed that HOCL can decompose the lipid hydroperoxides formed to yield alkoxyl radicals [170]. It was also suggested that chloramines formed in this process decompose to free radicals, which can initiate lipid peroxidation [171]. 

It follows from the above that MPO may catalyze the formation of chlorinated products in media containing chloride ions. Recently, Hazen et al. [172] have shown that the same enzyme catalyzes lipid peroxidation and protein nitration in media containing physiologically relevant levels of nitrite ions. It was found that the interaction of activated monocytes with LDL in the presence of nitrite ions resulted in the nitration of apolipoprotein B-100 tyrosine residues and the generation of lipid peroxidation products 9-hydroxy-10,12-octadecadienoate and 9-hydroxy-10,12-octadecadienoic acid. In this case there might be two mechanisms of MPO catalytic activity. At low rates of nitric oxide flux, the process was inhibited by catalase and MPO inhibitors but not SOD, suggesting the MPO initiation. 

The expression of 15-LOX in atherosclerotic lesions is one of the major causes of LDL oxidative modification during atherosclerosis. To obtain the experimental evidence of a principal role of 15-LOX in atherosclerosis under in vivo conditions, Kuhn et al. [67] studied the structure of oxidized LDL isolated from the aorta of rabbits fed with a cholesterol-rich diet. It was found that specific LOX products were present in early atherosclerotic lesions. On the later stages of atherosclerosis the content of these products diminished while the amount of products originating from nonenzymatic lipid peroxidation increased. It was concluded that arachidonate 15-LOX is of pathophysiological importance at the early stages of atherosclerosis. Folcik et al. [68] demonstrated that 15-LOX contributed to the oxidation of LDL in human atherosclerotic plaques because they observed an increase in the stereospecificity of oxidation in oxidized products. Arachidonate 15-LOX is apparently more active in young human lesions and therefore, may be of pathophysiological importance for earlier atherosclerosis. In advanced human plaques nonenzymatic lipid peroxidation products prevailed [69],... 

There are contradictory data on the effects of dietary ascorbic acid on free radical-mediated damage in animals. Barja et al. [65] found that the administration of 660mg/kg vitamin C to guinea pigs for 5 weeks significantly decreased the levels of protein carbonyls and lipid peroxidation products. On the other hand, the administration of 500mg/kg vitamin C to... 

It should be mentioned that the inhibition of superoxide overproduction and lipid peroxidation by lipoic acid has been recently shown in animal models of diabetes mellitus. The administration of LA to streptozotocin-diabetic rats suppressed the formation of lipid peroxidation products [213], In another study the supplementation of glucose-fed rats with lipoic acid suppressed aorta superoxide overproduction as well as an increase in blood pressure and insulin resistance [214]. 

The ALDs are a subset of the superfamily of medium-chain dehydrogenases/reductases (MDR). They are widely distributed, cytosolic, zinc-containing enzymes that utilize the pyridine nucleotide [NAD(P)+] as the catalytic cofactor to reversibly catalyze the oxidation of alcohols to aldehydes in a variety of substrates. Both endobiotic and xenobiotic alcohols can serve as substrates. Examples include (72) ethanol, retinol, other aliphatic alcohols, lipid peroxidation products, and hydroxysteroids (73). 

The LDL receptor has a much lower affinity for Lp(a) than for LDL. Therefore, the suggestion has been made that it is taken up by the scavenger pathway, preferentially after lipid peroxide products are formed by oxidation (HI). 

Romero, F.J., Bosch-MoreU, F., Romero, M.J., Jareno, E.J., Romero, B., Marin, N., and Roma, J., 1998, Lipid peroxidation products and antioxidants in human disease, Environ. Health Perspect. 106 Suppl 5 1229-1234... 

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